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Acetylation of VGLL4 Regulates Hippo-YAP Signaling and Postnatal Cardiac Growth

Z. Lin, H. Guo, Y. Cao, S. Zohrabian, P. Zhou, Q. Ma, N. VanDusen, Y. Guo, J. Zhang, SM. Stevens, F. Liang, Q. Quan, PR. van Gorp, A. Li, C. Dos Remedios, A. He, VJ. Bezzerides, WT. Pu,

. 2016 ; 39 (4) : 466-479. [pub] 20161006

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17023648
E-zdroje Online Plný text

NLK Cell Press Free Archives od 2001-07-01 do Před 1 rokem
Free Medical Journals od 2001 do Před 1 rokem
Elsevier Open Access Journals od 2001-07-01 do 2023-06-19
Elsevier Open Archive Journals od 2001-07-01 do Před 1 rokem

Odkazy

PubMed 27720608
DOI 10.1016/j.devcel.2016.09.005
Knihovny.cz E-zdroje

Binding of the transcriptional co-activator YAP with the transcription factor TEAD stimulates growth of the heart and other organs. YAP overexpression potently stimulates fetal cardiomyocyte (CM) proliferation, but YAP's mitogenic potency declines postnatally. While investigating factors that limit YAP's postnatal mitogenic activity, we found that the CM-enriched TEAD1 binding protein VGLL4 inhibits CM proliferation by inhibiting TEAD1-YAP interaction and by targeting TEAD1 for degradation. Importantly, VGLL4 acetylation at lysine 225 negatively regulated its binding to TEAD1. This developmentally regulated acetylation event critically governs postnatal heart growth, since overexpression of an acetylation-refractory VGLL4 mutant enhanced TEAD1 degradation, limited neonatal CM proliferation, and caused CM necrosis. Our study defines an acetylation-mediated, VGLL4-dependent switch that regulates TEAD stability and YAP-TEAD activity. These insights may improve targeted modulation of TEAD-YAP activity in applications from cardiac regeneration to cancer.

Citace poskytuje Crossref.org

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$a Binding of the transcriptional co-activator YAP with the transcription factor TEAD stimulates growth of the heart and other organs. YAP overexpression potently stimulates fetal cardiomyocyte (CM) proliferation, but YAP's mitogenic potency declines postnatally. While investigating factors that limit YAP's postnatal mitogenic activity, we found that the CM-enriched TEAD1 binding protein VGLL4 inhibits CM proliferation by inhibiting TEAD1-YAP interaction and by targeting TEAD1 for degradation. Importantly, VGLL4 acetylation at lysine 225 negatively regulated its binding to TEAD1. This developmentally regulated acetylation event critically governs postnatal heart growth, since overexpression of an acetylation-refractory VGLL4 mutant enhanced TEAD1 degradation, limited neonatal CM proliferation, and caused CM necrosis. Our study defines an acetylation-mediated, VGLL4-dependent switch that regulates TEAD stability and YAP-TEAD activity. These insights may improve targeted modulation of TEAD-YAP activity in applications from cardiac regeneration to cancer.
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$a Cao, Yuan $u Department of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Peking University, Fifth School of Clinical Medicine, Beijing 100730, China.
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